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The Korean journal of physiology & pharmacology : ... 14건

  1. [국내논문]   The Role of Adenosine Receptors on Acetylcholine Release in the Rat Striatum  

    Kim, Do-Kyung (Department of Pharmacology, Wonkwang University School of Medicine and Medicinal Resources Research Center of Wonkwang University ) , Kim, Hyeon-A (Department of Pharmacology, Wonkwang University School of Medicine and Medicinal Resources Research Center of Wonkwang University ) , Choi, Bong-Kyu (Department of Pharmacology, Wonkwang University School of Medicine and Medicinal Resources Research Center of Wonkwang University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 1 - 12 , 1997 , 1226-4512 ,

    초록

    As it has been reported that the depolarization induced acetylcholine (ACh) release is modulated by activation of presynaptic $A_1$ adenosine heteroreceptor and various evidence suggest that indicate the $A_2$ adenosine receptor is present in the striatum, this study was undertaken to delineate the role of adenosine receptors on the striatal ACh release. Slices from the rat striatum were equilibrated with $[^3H]$ choline and then the release amount of the labelled product, $[^3H]$ ACh, which was evoked by electrical stimulation (rectangular pulses, 3 Hz, 2 ms, 24 mA, $5\;Vcm^{-1}$ , 2 min), was measured, and the influence of various agents on the evoked tritium outflow was investigated. And also, quantitative receptor autoradiography and drug-receptor binding assay were performed in order to confirm the presence and characteristics of $A_1$ and $A_2$ adenosine receptors in the rat striatum. Adenosine $(10{sim}100\;{mu}M)$ and $N^6$ -cyclopentyladenosine (CPA, $1{sim}100\;{mu}M)$ decreased the $[^3H]$ ACh release in a dose-dependent manner without changing the basal rate of release in the rat striatum. The reducing effects of ACh release by adenosine and CPA were abolished by 8-cyclopentyl-1,3-dipropy-Ixanthine (DPCPX, 2 ${mu}M$ ), a selective $A_1$ , adenosine receptor antagonist, treatment. The effect of adenosine was potentiated markedly by 3,7-dimethyl-1-propargylxanthine (DMPX, 10 ${mu}M$ ), a specific $A_2$ adenosine receptor antagonist. 2-P-(2-carboxyethyl)phenethylamimo-5'-N- ethylcarboxamidoadenosine hydrochloride (CGS-21680C), in concentrations ranging from 0.01 to 10 ${mu}M$ , a recently introduced potent $A_2$ adenosine receptor agonist, increased the $[^3H]$ ACh release in a dose related fashion without changing the basal rate of release. These effects were completely abolished by DMPX $(10\;{mu}M)$ . In autoradiograrhy experiments, $[^3H]$ 2-chloro- $N^6$ -cyclopentyladenosine ($[^3H]$ CCPA) bindings were highly localized in the hippocampus and the cerebral cortex. Additionally, lower levels of binding were found in the striatum. However, $[^3H]$ CGS-21680C bindings were highly localized in the striatal region with the greatest density of binding found in the caudate nucleus and putamen. Lower levels of binding were also found in the nucleus accumbens and olfactory tubercle. In drug-receptor binding assay, binding of $[^3H]$ CCPA to $A_1$ adenosine receptors of rat striatal membranes was inhibited by CPA ( $K_i$ = 1.6 1.6 nM) and N-ethylcarboxamidoadenosine (NECA, $K_i$ = 12. 12.9 nM), but not by CGS-21680C ( $K_i$ = 260 2609.2 nM) and DMPX ( $K_i$ = 19, 19,386 nM). In contrast, $[^3H]$ CGS-21680C binding to $A_2$ denosine receptors was inhibited by CGS-21680C ( $K_i$ = 47. 47.6 nM) and NECA ( $K_i$ = 44. 44.9 nM), but not by CPA ( $K_i$ = 209 2099.2 nM) and DPCPX ( $K_i$ = 19, 19,207 nM). The results presented here suggest that both types of $A_1$ and $A_2$ adenosine heteroreceptors exist and play an important role in ACh release in the rat striatal cholinergic neurons.

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  2. [국내논문]   Regulation of Adenosine Receptors in Rat Brain following Chronic Carbamazepine Treatment  

    Park, Kyung-Sun (Department of Pharmacology and Institute of Basic Medical Sciences, Wonju College of Medicine, Yonsei University ) , Yang, Wan-Suk (Department of Pharmacology and Institute of Basic Medical Sciences, Wonju College of Medicine, Yonsei University ) , Kim, Kyung-Hwan (Department of Pharmacology, College of Medicine, Yonsei University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 13 - 17 , 1997 , 1226-4512 ,

    초록

    Carbamazepine (CBZ), an anticonvulsant, has beeen reported to displace ligands at adenosine receptors. Several studies have demonstrated that as far as $A_2$ adenosine receptors is concerned, CBZ acts as an antagonist. However, the situation with regard to Al receptors is less straightforward. In this study, we describe the effects of one-week CBZ treatment (25 mg/kg/day) on cerebrocortical $A_1$ adenosine receptors. $A_1$ adenosine receptor bindings as determined by using $[^3CH]DPCPX$ was not significantly altered in membranes prepared from CBZ-treated rats. However, there was a significant decrease in the $A_1$ adenosine receptor-mediated stimulation of $[^{35}S]GTP_{\gamma}S$ binding to cerebrocortical membranes prepared from CBZ-treated rats (20.0% decrease in basal activity; 17.8% decrease in maximal activity). The basal and $10^{-4}$ M forskolin-stimulated adenylyl cyclase activities were relatively unaffected by CBZ treatment, but 10 mM NaF-stimulated adenylyl cyclase activity was significantly reduced in CBZ-treated rats. It appears that one-week CBZ treatment caused an uncoupling of adenosine receptors from G proteins without alteration of $A_1$ adenosine receptor molecules, suggesting that CBZ acts as an agonist at $A_1$ adenosine receptors in rat brain.

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  3. [국내논문]   Enhanced Coupling of $M_1$ Muscarinic Receptors to Activation of Phospholipase C upon Mutation of a Transposed Amino Acid Triplet Repeat  

    Lee, Seok-Yong (Department of Pharmacology, Catholic University Medical College ) , Sung, Ki-Wug (Department of Pharmacology, Catholic University Medical College ) , Kim, Ok-Nyu (Department of Pharmacology, Catholic University Medical College ) , Lee, Sang-Bok (Department of Pharmacology, Catholic University Medical College)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 19 - 25 , 1997 , 1226-4512 ,

    초록

    The C-terminus ends of the second putative transmembrane domains of both $M_1$ and $M_2$ muscarinic receptors contain a triplet of amino acid residues consisting of leucine (L), tyrosine (Y) and threonine (T). This triplet is repeated as LYT-TYL in $M_1$ receptors at the interface between the second transmembrane domain and the first extracellular loop. Interestingly, however, it is repeated in a transposedfashion (LYT-LYT) in the sequence of $M_2$ receptors. In our previous work, we investigated the possible significance of this unique sequence diversity for determining the distinct differential receptor function at the two receptor subtypes. However, we found mutation of the LYTTYL sequence of $M_1$ receptors to the corresponding $M_2$ receptor LYTLYT sequence demonstrated markedly enhanced the stimulation of phosphoinositide (PI) hydrolysis by carbachol without a change in its coupling to increased cyclic AMP formation. In this work, thus, the enhanced stimulation of PI hydrolysis in the LYTLYT $M_1$ receptor mutant was further investigated. The stimulation of PI hydrolysis by carbachol was enhanced in the mutant $M_1$ receptor, and this change was not due to alterations in the rate of receptor desensitization or sequestration. The observed larger response to carbachol at mutant $M_1$ receptors was also not due to an artifact resulting from selection of CHO cells which express higher levels of G-proteins or phospholipase C. Our data suggest that although the LYTTYL sequence in $M_1$ muscarinic receptors is not involved in determining receptor pharmacology, mutation of the sequence enhanced the coupling of $M_1$ receptors to the stimulation of phospholipase C.

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  4. [국내논문]   Pharmacological Evidence that Cromakalim Inhibits $Ca^{2+}$ Release from Intracellular Stores in Porcine Coronary Artery  

    Rhim, Byung-Yong (Department of Pharmacology, College of Medicine, Pusan National University ) , Hong, Sun-Hwa (Department of Pharmacology, College of Medicine, Pusan National University ) , Kim, Chi-Dae (Department of Pharmacology, College of Medicine, Pusan National University ) , Lee, Won-Suk (Department of Pharmacology, College of Medicine, Pusan National University ) , Hong, Ki-Whan (Department of Pharmacology, College of Medicine, Pusan National University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 27 - 34 , 1997 , 1226-4512 ,

    초록

    In the present study, it was aimed to further indentify the intracellular action mechansm of cromakalim and levcromakalim in the porcine coronary artery. In intact porcine coronary arterial strips loaded with fura-2/AM, acetylcholine caused an increase in intracellular free $Ca^{2+}$ $([Ca^{2+}]_i)$ in association with a contraction in a concentration-dependent manner. Cromakalim (1 ${\mu}M$ ) caused a reduction in acetylcholine-induced increased $[Ca^{2+}]_i$ not only in the mormal physiological salt solution (PSS) but also in $Ca^{2+}$ -free PSS (containing 1 mM EGTA). In the skinned strips prepared by exposure of tissue to 20 . ${\mu}M$ B-escin, inositol 1,4,5-trisphosphate ( $IP_3$ ) evoked an increase in $[Ca^{2+}]_i$ , but it was without effect on the intact strips. The $IP_3$ -induced increase in $[Ca^{2+}]_i$ was inhibited by cromakalim by 78% and levcromakalim by 59% (1 . ${\mu}M$ , each). Pretreatment with glibenclamide (a blocker of ATP-sensitive $K^+$ channels, 10 . ${\mu}M$ ) and apamin (a blocker of small conductance $Ca^{2+}$ -activated $K^+$ channels, 1 . ${\mu}M$ ) strongly blocked the effect of cromakalim and levcromakalim. However, charybdotoxin (a blocker of large conductance $Ca^{2+}$ -activated $K^+$ channels, 1 . ${\mu}M$ ) was without effect. In addition, cromakalim inhibited the $GTP{\gamma}S$ (100 . ${\mu}M$ , non-hydrolysable analogue of GTP)-induced increase in $[Ca^{2+}]_i$ . Based on these results, it is suggested that cromakalim and levcromakalim exert a potent vasorelaxation, in part, by acting on the $K^+$ channels of the intracellular sites (e.g., sarcoplasmic reticulum membrane), thereby, resulting in decrease in release of $Ca^{2+}$ from the intracellular storage site.

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  5. [국내논문]   Effect of Cisplatin on Sodium-Dependent Hexose Transport in LLC-$PK_1$ Renal Epithelial Cells  

    Lee, Suk-Kyu (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College ) , Kim, Jee-Yeun (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College ) , Yu, Tai-Hyun (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College ) , Kim, Kyoung-Ryong (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College ) , Kim, Kwang-Hyuk (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College ) , Park, Yang-Saeng (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 35 - 43 , 1997 , 1226-4512 ,

    초록

    Cis-dichlorodiammine platin ${\mu}M$ II (Cisplatin), an effective chemotherapeutic agent, induces acute renal failure by unknown mechanisms. To investigate direct toxic effects of cisplatin on the renal proximal tubular transport system, LLC- $PK_1$ cell line was selected as a cell model and the sugar transport activity was evaluated during a course of cisplatin treatment. Cells grown to confluence were treated with cisplatin for 60 min, washed, and then incubated for up to 5 days. At appropriate intervals, cells were tested for sugar transport activity using ${\alpha}-methyl-D-[^{14}C]glucopyranoside$ (AMG) as a model substrate. In cells treated with 100 ${\mu}M$ cisplatin, the AMG uptake was progressively impaired after 3 days. The viability of cells was not substantially changed with cisplatin of less than 100 ${\mu}M$ , but it decreased markedly with 150 and 200 ${\mu}M$ . In cisplatin-treated cells, the $Na^+$ -dependent AMG uptake was drastically inhibited with no change in the $Na^+$ -independent uptake. Kinetic analysis indicated that Vmax was suppressed, but Km was not altered. The $Na^+$ -dependent phlorizin binding was also decreased in cisplatin-treated cells. However, the AMG efflux from preloaded cells was not apparently retarded by cisplatin treatment. These data indicate that the cisplatin treatment impairs $Na^+$ -hexose cotransporters in LLC- $PK_1$ cells and suggest strongly that defects in transporter function at the luminal plasma membrane of the proximal tubular cells constitute an important pathogenic mechanism of cisplatin nephrotoxicity.

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  6. [국내논문]   Gene Expression of Intrarenal Renin-angiotensin System in Streptozotocin-induced Diabetic Rats  

    Yang, Eun-Kyoung (Department of Physiology, School of Medicine, Kyungpook National University ) , Kim, In-Kyeom (Department of Pharmacology, School of Medicine, Kyungpook National University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 45 - 53 , 1997 , 1226-4512 ,

    초록

    In humans and many animal models with chronic progressive renal diseases, angiotensin-converting enzyme (ACE) inhibitor markedly attenuates the progression of nephropathy. Several studies have reported augmented gene expression and redistribution of renal renin in partial nephrectomized rats. Although precise mechanism(s) is not known, the renin-angiotensin system (RAS) may play an important role in the progression of renal diseases. Thus, this study was undertaken to examine the gene expression of renal renin, angiotensinogen, and $AT_1$ subtypes ( $AT_{1A}$ and $AT_{1B}$ ) in rats with diabetic nephropathy, and the influences of lipopolysaccharide (LPS)-induced septicemia on the gene expression. Four weeks after streptozotocin (STZ) treatment (55 mg/kg, i.p.), rats were randomly divided into LPS-treated (1.6 mg/kg, i.p.) and control rats. At 6 hours after LPS treatment, the rats were killed and the kidney was removed from each rat. Northern blot and reverse transcription-polymerase chain reaction (RT-PCR)techniques were used to detect mRNA expression. STZ treatment markedly attenuated body weight gain and significantly increased blood glucose level. Renal renin content (RRC) was significantly decreased in the STZ-treated rats compared to that in control rats. The renal ACE activity between STZ-treated and control rats was not significantly different. Renal renin mRNA level was prominently increased, while angiotensinogen and $AT_{1A}$ mRNA levels were slightly decreased in STZ-treated rats compared to those in controls. $AT_1$ B mRNA level did not differ in both groups. Acute LPS treatment did not show any significant changes of mRNA levels of intrarenal RAS components in both groups. These results suggest that intrarenal RAS components were differentially regulated in STZ-treated diabetic rats. Further studies are required to evaluate the relationship between intrarenal RAS and other vasomodulatory systems.

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  7. [국내논문]   Renal mRNA Expression of Renin, $AT_1$ Receptor, TGF-${\beta}1$ and Fibronectin in Obstructive Nephropathy  

    Yang, Eun-Kyoung (Department of Physiology, School of Medicine, Kyungpook National University ) , Kim, In-Kyeom (Department of Pharmacology, School of Medicine, Kyungpook National University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 55 - 63 , 1997 , 1226-4512 ,

    초록

    The present study was designed to quantify the alterations of renal renin, angiotensin type I receptor ( $AT_1$ ), $TGF-{\beta}1$ , and fibronectin gene expression in rats with unilateral ureteral obstruction (UUO). We also investigated the change of $AT_1$ density during UUO. Reverse transcription-polymerase chain reaction (RT-PCR) technique and receptor binding assay were used to detect mRNA expression and receptor density, respectively. At one day after UUO, renin mRNA level of the obstructed kidneys was decreased transiently and then subsequently increased to the level of sham kidneys. In the contralateral kidneys of the same rats, on the contrary, renin mRNA level was gradually decreased. Then, at 9 days after UUO, it was significantly lower than that of sham kidneys. The expressions of both $AT_1$ subtypes, called $AT_{1A}$ and $AT_{1B}$ , mRNAs did not change at any time. UUO led to a significant decrease in $AT_1$ density in the obstructed kidneys compared with the sham kidneys at 1 and 3 days $(66\;{\pm}\;11.6%\;(p (p $AT_1$ density was gradually increased and at 9 days it showed a marked elevation in the obstructed kidneys compared to the sham kidneys. In contrast, in the contralateral kidneys $AT_1$ density was significantly reduced from 3 to 9 days after UUO. The $TGF-{\beta}$ 1 mRNA level of the obstructed kidneys was unexpectedly decreased at 6 days after UUO. Then, at 9 days it was followed by a significant increase in the obstructed kidneys, whereas it showed an obvious decrease in the contralateral kidneys. In addition, fibronectin mRNA level was also significantly increased in the obstructed kidneys after UUO compared to the sham or the contralateral kidneys of the same rats. These results suggest a differential regulation of renal renin, $AT_1$ receptor, $TGF-{\beta}$ 1 and fibronectin mRNA levels at different stages of UUO.

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  8. [국내논문]   ANP Inhibits Surfactant Secretion from Isoproterenol Stimulated Alveolar Type II Cells  

    Lee, Young-Man (Department of Physiology, School of Medicine Catholic University of Taegu-Hyosung)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 65 - 70 , 1997 , 1226-4512 ,

    초록

    In order to investigate the effect of ANP on surfactant secretion from alveolar type II cell(AT II cell) during circulatory derangement in adult respiratory distress syndrome (ARDS), the secretion of surfactant from AT II cells was evaluated in purely isolated AT II cultures from rat lungs. For the simulation of sympathetic stimulation during circulatory derangement, primary AT II cultures were incubatedwith isoproterenol and IBMX. In this isoproterenol stimulated AT II cells, ANP were added in the media for the investigation of effect of ANP on surfactant secretion from AT II cells. For the evaluation of surfactant secretion, $[^3H]-methylcholine$ was incorporated and the level of radiolabelled choline chloride secreted from the cells was determined. As previously reported, isoproterenol and IBMX stimulated surfactant secretion from AT II cells. Isoproterenol showed synergistic increase of surfactant secretion with IBMX in AT II cells. In isoproterenol stimulated AT II cells, physiological level of ANP inhibited the secretion of surfactant in primary cultures of AT II cells. On the basis of these experimental it is suggested that, in association with ciculatory change during ARDS, increased secretion of ANP by the pulmonary edema, hypoxia and congestive heart heart failure might aggravate the symptoms of ARDS by reduction of surfactant secretion from AT II cells.

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  9. [국내논문]   Inhibition of Phospholipase $A_2$ Diminishes the Acute Alveolar Injury Induced by $Interleukin-1{\alpha}$  

    Lee, Young-Man (Department of Physiology, School of Medicine Catholic University of Taegu-Hyosung)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 71 - 78 , 1997 , 1226-4512 ,

    초록

    In an attempt to investigate the role of phospholipase $A_2$ ( $PLA_2$ ) in interleukin-l (IL-l) induced acute lung injury, mepacrine was tried to inhibit $PLA_2$ in IL-l induced ARDS rats. For confirmation of acute lung injury by IL-l, and to know the role of neutrophils in this injury, lung leak index, lung myeloperoxidase(MPO), number of neutrophils and protein content in the bronchoalveolar lavage (BAL) and wet lung weight were measured. At the same time lung $PLA_2$ was measured to know the effect of IL-l on $PLA_2$ activity. Pulmonary surfactant was also measured for an investigation of type II alveolar cell function. Neutrophil adhesion assay was performed to know the effect of $PLA_2$ inhibition in vitro with human umbilical vein endothelial cells (HUVEC). For precise location of injury by IL-l, morpholgical study was performed by electron microscopy. Five hours after instillation of IL-l (50 ng/rat), lung leak index, protein content, number of neutrophils, lung MPO and wet lung weight were increased significantly. Five hours after IL-l instillation lung $PLA_2$ activity was increased significantly, and increased surfactant release was observed in IL-l induced ARDS rats' BAL. In contrast, in rats given mepacrine and IL-l, there was decrease of acute lung injury i.e. decrease of lung leak index, wet lung weight, protein content, number of neutrophils in BAL and decreased lung MPO activity. Mepacrine decreased surfactant release also. Interestingly, inhibition of $PLA_2$ decreased adhesion of human neutrophils to HUVEC in vitro. Morphologically, IL-l caused diffuse necrosis of endothelial cells, type I and II epithelial cells and increased the infiltration of neutrophils in the interstitium of the lung but after mepacrine treatment these pathological findings were lessened. On the basis of these experimental results it is suggested that $PLA_2$ has a major role in the pathogenesis of acute lung injury mediated by neutrophil dependent manner in IL-l induced acute lung injury.

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  10. [국내논문]   Regulatory Role of Nitric Oxide on Atrial Natriuretic Peptide System in Normotensive and Hypertensive Rats  

    Choi, Eun-Hah (Department of Physiology, Chonnam University Medical School ) , Kim, Mi-Won (Department of Physiology, Chonnam University Medical School ) , Lee, Jong-Un (Department of Physiology, Chonnam University Medical School)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 79 - 82 , 1997 , 1226-4512 ,

    초록

    The present study was aimed to explore an interaction between endothelium-derived nitric oxide (NO) and atrial natriuretic peptide (ANP) systems in normotensive and hypertensive states. Rats were made two-kidney, one clip (2K1C) hypertensive and supplemented with either $N^G-nitro-L-arginine$ methyl ester (L-NAME, 5 mg/100 ml drinking water) or L-arginine hydrochloride (400 mg/100 ml drinking water). One group supplied with normal tap water served as control. Sham-clipped rats were also divided into the L-NAME, L-arginine, and control groups. The plasma levels and atrial contents of ANP were determined at day 28 following clipping the renal artery. In 2K1C rats, the plasma level of ANP was higher and the atrial content was lower than in the sham-clipped control. L-Arginine increased the atrial content of ANP in association with a decreased plasma ANP, whereas L-NAME significantly affected neither parameter. The increase of blood pressure in 2K1C rats was not affected by L-arginine or L-NAME. In sham-clipped rats, the plasma level of ANP was significantly increased by L-NAME along with an increase in blood pressure. On the contrary, L-arginine did not affect the blood pressure or plasma ANP. The atrial content of ANP was significantly altered neither by L-arginine nor by L-NAME. These results suggest that NO plays a tonic inhibitory role on the ANP release with concomitant increases of the atrial tissue content. In addition, hypertension is suggested to modify the release and tissue storage of ANP.

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